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Mitochondrial dysfunction is implicated in the pathology of neuronal damage during Alzheimer's disease (AD). Previous studies suggest that simvastatin (SV) ameliorates amyloid β (Aβ)‑mediated cognitive impairment in AD patients and transgenic mice; however, the mechanisms remain unknown. To investigate the potential mechanisms by which SV protects against AD neurotoxicity, the present study used a series of cellular and molecular assays to analyze the effects of SV in an in vitro model of Aβ1‑42-induced injury. The results demonstrated that SV protected against Aβ1‑42‑induced SH‑SY5Y cell injury by inhibiting the release of cytochrome c from the mitochondria to the cytoplasm, and reducing the production of intracellular reactive oxygen species. In addition, SV downregulated cleaved‑caspase‑3 protein levels, increased the ratio of B cell lymphoma 2 (Bcl-2) to Bcl-2-associated X protein, and increased the protein levels of peroxisome proliferator-activated receptor γ coactivator-1α in the Aβ1‑42‑treated cells. Furthermore, SV increased the mitochondrial membrane potential and adenosine triphosphate levels, and enhanced the cell respiratory function and mitochondrial mass of the cells. In conclusion, the present study revealed that SV protected SH‑SY5Y cells against Aβ1‑42-induced injury through regulating the mitochondrial apoptosis pathway and mitochondrial function.

Mitochondrial protective mechanism of simvastatin protects against amyloidï¿½β peptide-induced injury in SH-SY5Y cells